Studies of socially monogamous prairie voles reveal that pronounced individual differences in spatial memory structures (retrosplenial cortex and hippocampus) are better predictors of social and sexual fidelity than are areas known to regulate pairbonding directly, a pattern that seems to be mediated by the contributions of the neuropeptides to space use in natural settings. 
NPS receptors are predominantly expressed in the brain, especially in limbic structures, including amygdala, olfactory nucleus, subiculum and retrosplenial cortex. Also, MK-801 is known to produce histological changes such as cytoplasmic vacuoles in retrosplenial cortex neurons where NPS receptors are highly expressed. NPS treatment attenuated MK-801-induced vacuolization in the rat retrosplenial cortex in a dose-dependent manner that can be blocked by an NPS receptor-selective antagonist. NPS also suppressed MK-801-induced increases of extracellular acetylcholine levels in the retrosplenial cortex.
Persistent changes were assessed in glucocorticoid receptor density and Fos activity in the anterodorsal thalamic nuclei, mammillary nuclei and retrosplenial cortex.
More interestingly however perfusion increases were observed in a few cortical and subcortical regions of the contralateral hemisphere: the supplementary motor area, the primary somatosensory area, the posterior insula and posterior putamen, the hippocampus and bilaterally the retrosplenial cortex.
Here, we investigate mechanisms of bundle formation, focusing on layer (L) 2 bundles in rat granular retrosplenial cortex (GRS), a limbic area implicated in spatial memory.
Both the retrosplenial cortex (RSC) and the hippocampus are important for spatial learning across species.
A potential clue comes from the dense, reciprocal connections between the anterior thalamic nuclei and retrosplenial cortex, another region vital for memory. We now report a loss of synaptic plasticity [ long-term depression (LTD)] in rat retrosplenial cortex slices months following an anterior thalamic lesion. As retrosplenial cortex is itself vital for memory, this distal lesion effect will amplify the impact of anterior thalamic lesions.
In this paper, we report functional magnetic resonance imaging (fMRI) evidence that these distinct computations may occur in two scene-sensitive regions in the brain, the parahippocampal place area (PPA) and retrosplenial cortex (RSC).
The present study of the connections of the STG with medial paralimbic cortex showed that the caudal part of the STG (area Tpt and caudal area paAlt) and adjacent cortex of the upper bank of the superior temporal sulcus (caudal area TPO) have reciprocal connections with the caudal cingulate gyrus (areas 23a, b and c), retrosplenial cortex (area 30), and area 31.
Rather, RT improvements were directly correlated with repetition enhancement in the hippocampus and the posteromedial cortex [ posterior cingulate cortex, precuneus, and retrosplenial cortex; Brodmann's areas (BAs) 23, 7, and 30, respectively], regions known to support memory formation and retrieval, and in the SMA (BA 6) and the dorsal midcingulate ("motor cingulate") cortex (BA 24d), regions known to be important for motor learning.
Functional magnetic resonance imaging (fMRI) revealed that, relative to speech-modulated noise, voices rated as familiar and unfamiliar by MS elicited enhanced haemodynamic activity in the left angular gyrus, left posterior STS, and posterior midline brain regions, including the retrosplenial cortex and the dorsal pCG.
The retrosplenial cortex consists of areas 29a-d, each of which has different connections with other cortical and subcortical regions. In the study reported here, we investigated the organization of associational and commissural connections of areas 29a-d within the retrosplenial cortex in the rat, using the retrograde tracer cholera toxin B subunit and anterograde tracer biotinylated dextran amine. The results demonstrated that each of these areas has a distinct set of interconnections within the retrosplenial cortex. Each area interconnects strongly along the transverse axis of the retrosplenial cortex: area 29a, area 29b, caudal area 29c, and caudal area 29d connect with each other, and rostral area 29c and rostral area 29d connect with each other.
Contrast D-V revealed a mainly parieto-hippocampal network comprising precuneus and inferior parietal cortex, posterior parieto-occipital cortex, retrosplenial cortex and the hippocampal region, but also right superior frontal gyrus and right cerebellum.
Decreased activity, as measured by immediate-early gene expression (c-fos), was found in three key sites associated with memory function: the hippocampus, the prefrontal cortex, and the retrosplenial cortex. The specificity of these changes was confirmed by the qualitatively different patterns of immediately-early gene changes seen after amygdala lesions, e.g., hypoactivity in the hippocampus and retrosplenial cortex following mammillothalamic tract lesions but not following amygdala lesions.
However, medially a transition zone of intermediate intensity was found between primarily visual, that is V1 and multimodal retrosplenial cortex.
Four experiments examined the disruptive effects of selective lesions in limbic thalamic nuclei on retrosplenial cortex function, as characterized by striking changes in immediate-early gene activity. Experiment 1 examined the activity of two immediate-early genes (c-Fos, Zif268) in the retrosplenial cortex after unilateral anterior thalamic nuclei lesions (1, 2, or 8 weeks post-surgery). The results confirmed that over time the immediate-early gene disruption expanded from the superficial laminae to the deep laminae of granular b cortex and to the dysgranular subregion, indicative of more global disruptions to retrosplenial cortex with extended survival. Associated, subtle changes to cell morphometry (size and sphericity) were found in the retrosplenial cortex. In contrast, unilateral lesions in the adjacent laterodorsal thalamic nucleus (Experiment 4) did not significantly alter retrosplenial cortex c-Fos activity, so highlighting the anatomical specificity of the anterior thalamic lesion effects. These findings not only indicate that the impact of anterior thalamic lesions on cognition could be enhanced by retrosplenial cortex dysfunction but they also show that the effects could increase with longer post-insult survival..
These uncharacteristically prolonged responses were not limited to the remapped peri-infarct zone and included distant posteromedial retrosplenial cortex, millimeters from the stroke. Structurally, the remapped peri-infarct area selectively exhibited high levels of dendritic spine turnover, shared more connections with retrosplenial cortex and striatum, and lost inputs from lateral somatosensory cortical regions.
Overexpression of IL-1ra was found to reduce the basal as well as the novelty-induced upregulation of activity-regulated cytoskeleton-associated protein (Arc) in the dentate gyrus and in the retrosplenial cortex.
Volumes of medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), retrosplenial cortex (RSC) and hippocampal formation were compared between groups and with behavioral measures, i.e.
In contrast, lesions to the retrosplenial cortex impaired performance on a spatial navigation task and the classic radial maze.
Recent compared to early childhood events activated retrosplenial cortex.
Reversal of MK801 toxicity was complete in the caudate-putamen, partial in the somatosensory cortex but was not observed in the retrosplenial cortex.
Increased number of glial fibrillary acidic protein immunopositive cells in the retrosplenial cortex or throughout the hippocampus revealed an Abeta(25-35)-induced inflammation that was prevented by ANAVEX1-41.
The retrosplenial cortex is seen as a convergence point for different classes of spatial cue, yet aside from allocentric processing, little is known about other cue types that depend on the integrity of this area. Rats with bilateral retrosplenial cortex lesions were, therefore, trained on a sequence of reinforced spatial alternation tasks designed to isolate different spatial strategies. retrosplenial cortex lesions only disrupted the latter (direction alternation) condition. The pattern of findings in the present study strongly indicates that retrosplenial cortex lesions impair the use of direction cues for alternation, in addition to previously established impairments for allocentric-based navigation and path integration..
Mounting evidence indicates that the retrosplenial cortex (RSP) has a critical role in spatial navigation.
hippocampus, forebrain cortex, anterior cingulate, retrosplenial cortex) and the anterior thalamic nuclei that bridge the motor and cognitive components of aggressive responding.
Distinct sub-regions within dorsal and ventral medial prefrontal cortex, retrosplenial cortex and along the parieto-occipital sulcus preferentially coded for events (real or imagined) involving the self. Taken together our results permitted a functional deconstruction of anterior (medial prefrontal) and posterior (retrosplenial cortex, posterior cingulate cortex, precuneus) cortical midline regions widely associated with autobiographical memory but whose roles have hitherto been poorly understood..
Consistent with the hypothesis that REMs share the brain systems and mechanisms with waking eye movements and are visually-targeted saccades, we found REM-locked activation in the primary visual cortex, thalamic reticular nucleus (TRN), 'visual claustrum', retrosplenial cortex (RSC, only on the right hemisphere), fusiform gyrus, anterior cingulate cortex, and the oculomotor circuit that controls awake saccadic eye movements (and subserves awake visuospatial attention).
retrosplenial cortex (RSC) together with the hippocampus is a component of the spatial memory circuit. Our results suggest an involvement of retrosplenial cortex in the segregation of spatial information..
Our laboratory recently demonstrated that electrolytic lesions of the retrosplenial cortex (RSP), a posterior region of cingulate cortex, impaired contextual but not cue-specific fear conditioning.
Consistent with the patient's behavioural findings, a functional magnetic resonance imaging (fMRI) study showed lack of activation in the hippocampal complex and the retrosplenial cortex while forming a cognitive map of the environment. First, in a group of healthy control subjects performing the same task, activity within the hippocampal complex and retrosplenial cortex were detected in each individual participant.
An extensive cortical network consisting of structures in the medial temporal lobe (hippocampus and parahippocampal cortex), lateral parietal cortex, retrosplenial cortex, and medial prefrontal cortex has recently attracted attention in cognitive neuroscience research, linking the network to both episodic memory and spatial processing. Functional magnetic resonance imaging during encoding yielded significant activations in all regions of the context network, i.e., medial prefrontal cortex, lateral parietal cortex, retrosplenial cortex, and posterior medial temporal lobe for the associative vs.
Seizures induced by hippocampal stimulation produced a similar pattern, and were used to perform functional magnetic resonance imaging weighted for blood oxygenation and blood volume, demonstrating increased signals in hippocampus, thalamus and septum, but decreases in orbitofrontal, cingulate, and retrosplenial cortex during partial seizures, and increases in all of these regions during propagated seizures.
This study investigates by functional MRI (fMRI) the characteristics of processing activities at the retrosplenial cortex (RSC) and compares them to activities at the parahippocampal place area (PPA).
In retrosplenial cortex, less Fos expression occurred in F vs.
Errors also evoked greater activity in the cuneus, retrosplenial cortex, insula, and subcortical structures including the thalamus and the region of the epithalamus (the habenula).
A third development is the possibility that the retrosplenial cortex provides an integrating link in this functional system. Furthermore, recent evidence indicates that the retrosplenial cortex may suffer "covert" pathology (i.e., it is functionally lesioned) following damage to the anterior thalamic nuclei or hippocampus. This shared indirect "lesion" effect on the retrosplenial cortex not only broadens our concept of the neural basis of amnesia but may also help to explain the many similarities between temporal lobe and diencephalic amnesia..
Execution of reaching-to-grasp induced activations in the superior parietal areas SI-forelimb/convexity, PE, PE caudal (PEc); in the intraparietal areas PE intraparietal (PEip), medial intraparietal (MIP), 5 intraparietal posterior, ventral intraparietal (VIP), anterior intraparietal (AIP), lateral intraparietal dorsal; in the inferior parietal areas PF, PFG, PG; in the parietoccipital areas V6, V6A-dorsal; in the medial cortical areas PGm/7m and retrosplenial cortex. Observation of reaching-to-grasp activated areas SI-forelimb/convexity, PE lateral, PEc, PEip, MIP, VIP, AIP, PF, V6, PGm/7m, 31, and retrosplenial cortex.
Retrograde and anterograde amnesic effects of excitotoxic lesions of the rat retrosplenial cortex (RS) and hippocampus (HPC) were investigated.
In order to address this, we documented the effect of nbm corticopetal cholinergic lesions on cortical activity in direct (prefrontal cortex) and indirect (retrosplenial cortex) targets of nbm corticopetal cholinergic neurons during footshock induced operant suppression.
Patients with MDD had significantly reduced reward-learning signals in many non-brainstem regions: ventral striatum (VS), rostral and dorsal anterior cingulate, retrosplenial cortex (RC), midbrain and hippocampus.
Low doses induce behavioral disturbances and higher doses, in addition, promote neurotoxicity in many brain regions, particularly the granular retrosplenial cortex (RSG).
Incipient AD showed GM atrophy in the medial temporal and temporoparietal lobes, in the insula and in the retrosplenial cortex, and GM hypoperfusion in the medial temporal and temporoparietal lobes.
MK801 (dizocilpine) induces selective neurotoxic effects in the retrosplenial cortex, ranging from neuronal vacuolization to irreversible neurodegeneration depending on the dose administered. Although lamotrigine prevents MK801-induced neuronal vacuolization in the retrosplenial cortex 4 h after injection, it is not clear whether lamotrigine attenuates the subsequent neurodegeneration that occurs 3-4 days later. Because early growth response factor-1 (egr-1) plays a key role in neurodegeneration and its expression is induced in the retrosplenial cortex following MK801 treatment, it is possible that lamotrigine may attenuate MK801-induced neurodegeneration via inhibition of egr-1 expression in the retrosplenial cortex. To address this issue, we treated rats with lamotrigine (10 or 20 mg/kg) followed by MK801 (2 mg/kg) and measured changes in the levels of egr-1 mRNA and immunoreactivity in the retrosplenial cortex and other brain regions 3 h later. In addition, MK801-induced neurodegeneration in the retrosplenial cortex was partially blocked by lamotrigine pretreatment in a dose dependent manner. These results demonstrate that lamotrigine pretreatment prevents the MK801-induced upregulation of egr-1 expression in a region-selective manner, and suggest that this effect may contribute, in part, to the attenuation of MK801-induced neurodegeneration in the retrosplenial cortex..
The effect was specific for the hippocampal formation, with levels of alpha1d mRNA unaltered by ADX in the lateral amygdala, reticular thalamic nucleus, retrosplenial cortex or primary somatosensory cortex.
Lesions of retrosplenial cortex (RSP) disrupt spatial and contextual learning, suggesting that RSP may have a fundamental role in processing overlapping, or simultaneously presented stimuli.
Across all domains, and consistent with the proposed network, correspondence was found within the medial-temporal lobe, precuneus, posterior cingulate, retrosplenial cortex, and the temporo-parietal junction.
Visual, sensory-motor, auditory, and retrosplenial cortex showed modulations of the BOLD spectral density by resting state type.
Axonal degeneration was followed by profound apoptotic cell death in the posterior cingulate and retrosplenial cortex and anterior thalamus which peaked between 16 and 24 h post-injury.
Using seed regions from the functional connectivity maps, the DTI analysis revealed robust structural connections between the MTLs and the retrosplenial cortex whereas tracts from the MPFC contacted the PCC (just rostral to the RSC).
It is now becoming possible to construct a mechanistic neural-level model of at least some aspects of spatial memory and imagery, with the hippocampus and medial temporal lobe providing allocentric environmental representations, the parietal lobe egocentric representations, and the retrosplenial cortex and parieto-occipital sulcus allowing both types of representation to interact.
This case suggested that dementia is brought on by the lesion of the left posterior cingulate bundle and retrosplenial cortex causing amnesia by disrupting the cingulate-hippocampal connection or the retrosplenial cortex itself, with the lesion of the left occipitoparietal subcortex causing frontal dysfunction by disrupting the dorsal limbic pathway and occipitofrontal fasciculus of the prefrontal circuits..
The body of the hippocampus and posterior parahippocampal cortex correlated with lateral parietal cortex, regions along the posterior midline including posterior cingulate and retrosplenial cortex, and ventral medial prefrontal cortex.
Injections of Abeta into the retrosplenial cortex resulted in a decrease in alpha7nAChR-immunoreactivity in the hippocampus.
The neuronal density and apoptosis in CA1 and dentate gyrus of hippocampus, prefrontal cortex, parietal cortex, subiculum, and retrosplenial cortex were assessed by immunohistochemistry and ELISA cell death assay.
During correct recognition of studied words (true memory), older adults showed weaker activity than young adults in the hippocampus but stronger activity than young adults in the retrosplenial cortex.
The retrosplenial cortex (RSP) and the posterior parietal cortex (PPC) are the primary sources of cortical sensory input to the postrhinal cortex (POR) in rodents.
Cells projecting to the orofacial and forelimb areas of M1 were distributed in the anterior cingulate cortex (area 24) but not in the posterior cingulate cortex (retrosplenial cortex; area 29), according to topographical mapping.
Electrophysiological and neuroanatomical analyses revealed also that LD projects upon the cingulate and retrosplenial cortex, but has only sparse projections to the barrel cortex.
RESULTS: Injections of A beta into the retrosplenial cortex resulted in a significant reduction in M2mAChR-immunoreactivity in the CA1 ipsilateral to the A beta-injected side as compared with the corresponding hemisphere of non-treated control animals and with that in the corresponding region of the CA1 in the phosphate-buffered saline-injected side.
In contrast, V1aR expression in the posterior cingulate/retrosplenial cortex (PCing) and laterodorsal thalamus (LDThal), areas implicated in spatial memory, strongly covaried with space use and paternity.
Particularly, dyslexics showed main activity being located at posterior cingulate cortex (Brodmann's area 31) while controls exhibited main activity being located at retrosplenial cortex (Brodmann's area 30).
In Ts65Dn, but not Ts1Cje mice, transverse proton spin-spin (T(2)) relaxation time was selectively reduced in the medial septal nucleus (MSN) and in brain regions that receive cholinergic innervation from the MSN, including the hippocampus, cingulate cortex, and retrosplenial cortex.
This was associated with activations in a distributed network, including hippocampus, parahippocampal gyrus, and retrosplenial cortex.
This system, which is also connected with the entorhinal, parahippocampal, and cingulate/retrosplenial cortex, may be involved in emotion and other self-referential processes..
The role of the primate retrosplenial cortex (RSC) in memory processing and spatial navigation has been well established.
Visceronociceptive neurons were most frequent in ACC (39%) and midcingulate cortex (MCC, 36%) and infrequent in retrosplenial cortex (RSC, 12%).
The retrosplenial cortex (areas 29a-d), which plays an important role in spatial memory and navigation, is known to provide massive projections to frontal association and motor cortices, which are also essential for spatial behavior. These differential frontal cortical projections to each area of the retrosplenial cortex suggest that each area may contribute to different aspects of retrosplenial cortical function such as spatial memory and behavior..
RESULTS : In comparison with normal controls, amnestic MCI patients who converted to AD showed hypoperfusion in the right parahippocampal gyrus and left inferior temporal and fusiform gyri,whereas those who did not convert showed hypoperfusion in the retrosplenial cortex, precuneus and occipital gyri, mainly on the left side.We found no overlap between significant atrophy and significant hypoperfusion regions. CONCLUSIONS : Parahippocampal and inferior temporal hypoperfusion in amnestic MCI patients appears as a correlate of conversion to AD; hypoperfusion in the retrosplenial cortex is involved in memory impairment but does not seem the key prognostic indicator of conversion to dementia..
Similar results were observed in the secondary auditory cortex; however, there were no significant changes in Fos expression in other auditory or visual cortices or in other cortical association areas that have been implicated in attentional function (frontal, cingulate or retrosplenial cortex).
Hippocampal-lesioned animals only showed hypometabolism in the retrosplenial cortex.
The dorsomedial limbic stream via the cingulate fasciculus targets the anterior and posterior cingulate cortex, as well as the retrosplenial cortex, allowing control over motivational and memory processes.
Rat fetal exposure to isoflurane at pregnancy day 21 through maternal anesthesia significantly decreased spontaneous apoptosis in the hippocampal CA1 region and in the retrosplenial cortex at 2h after exposure, but not at 18h or at P5.
Old rats only show decreases in the number of PSA-NCAM expressing cells in the lateral amygdala and retrosplenial cortex, and in neuropil expression of stratum lucidum.
The present study examined whether hippocampal lesions disrupt retrosplenial cortex function. The immediate-early genesc-fos and zif268 provided markers of cellular activity, and their levels were compared in different cytoarchitectonic subregions (dysgranular, granular a and granular b) and different layers (superficial or deep) within retrosplenial cortex. Experiments 1-3 examined the impact of hippocampal lesions on retrosplenial cortex function, with the variations in protocol (e.g. Despite the loss of Fos and Zif268, there was no evidence of retrosplenial cortex atrophy as measured by Nissl counts (experiments 1-3) or NeuN-positive cell counts (experiment 3). These results provide strong support for the notion that the retrosplenial cortex is unusually sensitive to deafferentation from some of its inputs, so that hippocampal damage might produce permanent 'covert pathology' in the retrosplenial cortex.
The retrosplenial cortex (RS) in rats has been implicated in a wide range of behaviors, including spatial navigation and memory. Here, by injecting the retrograde tracer cholera toxin subunit B conjugated with Alexa488 (CTB-Alexa488) in the granular retrosplenial cortex (GRS), we demonstrate a moderately dense non-pyramidal projection from CA1.
We examined the behavior of electrically evoked signals from primary visual cortex (Oc1) to granular retrosplenial cortex (RSG) in rat brain slices under caffeine application. With continued electrical stimulation, evoked signals propagated from Oc1 to RSG along the upper layer of the secondary visual cortex (Oc2) and agranular retrosplenial cortex (RSA), but on further continuation of stimulation, a new shortcut pathway along the deep layer between Oc2 and RSG was opened.
The rat granular retrosplenial cortex (GRS) is a simplified cortex, with distinct stratification and, in the uppermost layers, distinct modularity.
Finally, a large population of somatostatin-negative GABAergic cells in stratum radiatum project to the molecular layers of the subiculum, presubiculum, retrosplenial cortex, and indusium griseum and fire rhythmically at high rates during theta oscillations but do not increase their firing during ripples. Other areas, including the retrosplenial cortex, receive only rhythmic GABAergic CA1 input.
The medial network has outputs to the hypothalamus and brain stem and connects to a cortical circuit that includes the rostral part of the superior temporal gyrus and dorsal bank of the superior temporal sulcus, the cingulate and retrosplenial cortex, the entorhinal and posterior parahippocampal cortex, and the dorsomedial prefrontal cortex..
In regions such as the cingulate and retrosplenial cortex, injury peaks at postnatal Day 7 (P7) and rapidly diminishes thereafter, whereas expression of calbindin (CB) and calretinin (CR) was relatively low from P0 to P7 and steadily increased from P7 to P14.
Autobiographical episodic versus semantic memory retrieval in the controls led to significant bilateral activations of the parietal-temporal junction, left temporal pole, anterior cingulate, retrosplenial cortex and cerebellum. In MCI patients compared to controls a dysfunction of the retrosplenial cortex during memory retrieval was revealed by a lack of differential activation in relation to recency of memories and memory type.
We used fMRI to directly compare activation in two cortical regions previously identified as relevant to real-world scene processing: retrosplenial cortex and a region of posterior parahippocampal cortex functionally defined as the parahippocampal place area (PPA). In contrast, activation in retrosplenial cortex was greatest for full scene views, and did not differ among close-up views, diagnostic objects, and faces. The results showed that parahippocampal place area responds in a graded fashion as images become more completely scene-like and include more explicit 3D structure, whereas retrosplenial cortex responds in a step-wise manner to the presence of a complete scene.
Four scene-selective regions (lateral precuneus, retrosplenial cortex, PPA, and middle occipital gyrus) showed an anatomical gradient of responsiveness to top-down reflective influences versus bottom-up perceptual influences.
Our analyses focused on the retrosplenial cortex (RSC)/parietal-occipital sulcus region and the parahippocampal place area (PPA), which previous studies indicate play a critical role in place recognition.
Our findings indicate that treatment of adult rats with MK801 in doses previously found to cause alterations in pyramidal neurons of the retrosplenial cortex (5mg/kg) results in an active caspase 3 (+), ultrastructurally apoptotic type of cell death involving the same projection neurons of layer IIalpha that are also vulnerable to bulbotomy lesions.
Consistent with behavioral reports, we observed boundary extension for scene-selective attenuation in the parahippocampal place area (PPA) and retrosplenial cortex (RSC), but no such extrapolation of object representations in the lateral occipital complex (LOC).
Major projections from the retrosplenial cortex were directed to the frontal lobe, with heaviest terminations in areas 46, 9, 10, and 11.
Scene-selective regions in parahippocampal cortex (the parahippocampal place area, or PPA), retrosplenial cortex (RSC), and the transverse occipital sulcus (TOS) responded more strongly to images of familiar locations than to images of unfamiliar locations with the strongest effects (>50% increase) in RSC.
In addition it had extensive connections with limbic regions including the amygdala, parahippocampal cortex, cingulate, and retrosplenial cortex..
The retrosplenial cortex is a cytoarchitecturally distinct brain structure located in the posterior cingulate gyrus and bordering the splenium, precuneus, and calcarine fissure.
We combined functional magnetic resonance imaging with a virtual-reality paradigm to investigate the functional interaction of the hippocampus and retrosplenial cortex during the formation and utilization of cognitive maps by human subjects. In conjunction with the hippocampus, the retrosplenial cortex was active during both the formation and the use of the cognitive map. In accordance with earlier studies in non-human animals, these findings suggest that, while navigating within the environment, the retrosplenial cortex complements the hippocampal contribution to topographical orientation by updating the individual's location as the frame of reference changes..
Injections of Abeta protein into the retrosplenial cortex resulted in a decrease in M1mAChR and M2mAChR immunoreactivity in the MS-nDBB complex.
In LOAD, GM loss was diffusely milder (below 15%); losses of 15-20% were confined to temporoparietal and retrosplenial cortex, and reached 25% in restricted areas of the medial temporal lobe and right superior temporal gyrus.
We identified a transition zone from NR2C-expressing neurons to astrocytes in an area connecting the retrosplenial cortex and hippocampus. We also demonstrate novel areas of neuronal expression such as retrosplenial cortex, thalamus, pontine and vestibular nuclei.
On the contrary, increases in alpha(1)-adrenoceptors after 2-h withdrawal were seen in the nucleus accumbens core and retrosplenial cortex. In cocaine-sensitized rats, the density of alpha(1)-adrenoceptors 2 h after the challenge with cocaine increased in the centrolateral amygdala, while in the granular retrosplenial cortex and in the most of thalamic nuclei, the densities of alpha(1)-adrenoceptors decreased.
Non-competitive N-methyl-D-aspartate (NMDA) antagonists (MK-801 and phencyclidine) increase glucose metabolism in many brain areas and induce cytoplasmic vacuoles, heat shock protein and necrotic cell death in neurones of the rodent posterior cingulate and retrosplenial cortex. Free radical scavengers (dimethyl sulfoxide (DMSO) and alpha-tocopherol) and spin traps (N-tert-butyl-alpha-(2-sulfophenyl)-nitrone (S-PBN) and 5-(diethoxyphosphoryl)-5-methyl-1-pyrrole N-oxide (DEPMPO)), produced marked attenuation of MK-801-induced neuronal necrosis in the rat posterior cingulate and retrosplenial cortex.
Prior studies identify two cortical areas, posterior parahippocampal cortex and retrosplenial cortex, that preferentially activate to images of real-world scenes compared to images of other meaningful visual stimuli such as objects and faces. In contrast, no such difference was observed in retrosplenial cortex, though this region preferentially activated to scenes over faces.
Comparisons with a control group revealed discrete decreases in Fos centred in the hippocampus and retrosplenial cortex. The selective immediate-early gene changes in the hippocampus and two closely related sites (retrosplenial cortex and anterior ventral thalamic nucleus) when processing the new stimulus configuration support the notion that the hippocampus is important for learning the 'relational' or 'structural' features of arrays of elements, be they spatial or temporal..
In Experiment 1, increased activation was observed within the anterior frontomedian cortex (aFMC), precuneus, and retrosplenial cortex when participants followed the RH compared to when they did not.
During postnatal development the distribution of alpha2 subunit mRNA expression was spatially similar to the one found in adult, exhibiting highly restricted expression in scattered cells mostly in cortical layer V and retrosplenial cortex, and in scattered cells in CA1/CA3 stratum oriens and CA3 stratum radiatum.
PbTx-3 inhalation exposure produced neuronal degeneration in the posterior cingulate/retrosplenial cortex of mice as evidenced by silver-positive degenerating neurons in this region. Fluro-Jade-positive neurons were observed in the retrosplenial cortex of PBTx-3 exposed, but not control, mice.
Quantitative analyses demonstrate that the representation of the far periphery receives specific connections from the retrosplenial cortex (areas 23v and prostriata), as well as comparatively stronger inputs from the primary visual area (V1) and from areas surrounding MT (in particular, the medial superior temporal area, MST).
Scene-responsive voxels in the parahippocampal place area (PPA) and retrosplenial cortex (RSC) were highly sensitive to recognition level when identifying scenes, responding more strongly during location identification than during place category or situation identification.
MK-801 induces cytoplasmic vacuoles and heat shock protein in pyramidal neurones in the rodent posterior cingulate and retrosplenial cortex.
In neurochemical and electrophysiological correlates of antipsychotic drug action, SSR180711 increased extracellular levels of dopamine in the prefrontal cortex (MED: 1 mg/kg) and enhanced (3 mg/kg) spontaneous firing of retrosplenial cortex neurons in rats.
In the absence of task, stimuli, or explicit mnemonic demands, robust correlations were observed between activity in the HF and several parietal regions (including precuneus, posterior cingulate, retrosplenial cortex, and bilateral inferior parietal lobule).
Valproate pretreatment significantly blocked the MK801-induced increase of BDNF expression in retrosplenial cortex at 3 h, 6 h, and 9 h after MK801 injection, suggesting that valproate pretreatment did not delay the MK801-induced increase of BDNF expression.
There is strong evidence that the rat retrosplenial cortex (RC) is implicated in spatial navigation and in learning of both aversive and reward-based discrimination tasks.
The first major wave of apoptotic neurodegeneration occurred at 8 h postimpact in the retrosplenial cortex and pre- and parasubiculum.
This later surge in expression was especially true for parvalbumin in regions such as the somatosensory and retrosplenial cortex, as well as the subicular complex.
The right posterodorsal posterior cingulate cortex (pPCC) and left retrosplenial cortex, whose involvement in place-recognition has been previously established, were selected as regions of interest for the PCA. Neural responses to objects associated with familiar relative to unfamiliar places in pPCC, but not in the retrosplenial cortex, were negatively correlated with task-related activation (common over all objects) in the right anterolateral prefrontal cortex and the left intraparietal sulcus. These results suggest right prefrontal control over neural processes both in the left parietal cortex, related to object-recognition (enhancement), and pPCC, related to nonessential recollection of place-memory (suppression), but not in the retrosplenial cortex, related to the sense of familiarity.
Head direction (HD) cells located in several regions of the brain, including the postsubiculum, retrosplenial cortex, lateral dorsal thalamic nucleus, anterior dorsal thalamic nucleus, and lateral mammillary nucleus, provide a signal of the rat's momentary directional heading.
The retrosplenial cortex showed a twofold greater increase in activity as compared with other cortical areas, also peaking at approximately 15 s. The anterior thalamus and retrosplenial cortex were essentially blocked by pretreatment with ESM. CONCLUSIONS: The anterior thalamus, retrosplenial cortex, and dentate gyrus show the greatest increases in BOLD signal activity before seizure onset.
In both groups of listeners, minor and dissonant chords, compared with major chords, elicited enhanced responses in several brain areas, including the amygdala, retrosplenial cortex, brain stem, and cerebellum, during passive listening but not during memorization of the chords.
Among 12 structures expressing postsynaptic 5-HT1AR in wild-type neonates, the highest densities involved the retrosplenial cortex, entorhinal cortex, and septum (52-46 fmol/mg tissue); low densities occurred in the hippocampus and spinal cord (24 fmol/mg tissue); in addition, the raphe autoreceptor density was only 20 fmol/mg tissue.
The rat retrosplenial cortex is part of a heavily interconnected limbic circuit, considered to have an important role in spatial memory. Interestingly, the granular retrosplenial cortex has an exceptionally distinct system of dendritic bundles, originating from callosally projecting pyramidal neurons in layer II. These can be detected as early as postnatal day 5; and, although their functional significance remains to be elucidated, the existence of these bundles makes the granular retrosplenial cortex an attractive model system for a wide range of development and functional investigations. Here, we report four results concerning the development of modularity in the granular retrosplenial cortex in rats as investigated by neurochemical markers associated to cortico-cortical and thalamo-cortical connections.
The present study provides the 1st report on the effects of selective lesions of the dysgranular portion of the retrosplenial cortex in rats. This change in strategy is consistent with anatomical data showing that the dysgranular region is the primary recipient of visual inputs to the rat retrosplenial cortex..
All 4 cingulate regions were significantly smaller (P < 0.05) in AD cases compared with controls: rostral anterior cingulate gyrus (22.5% smaller), caudal anterior cingulate gyrus (20.7% smaller), posterior cingulate gyrus (44.1% smaller), and retrosplenial cortex (21.5% smaller).
However, reduced rCBF was additionally found in the retrosplenial cortex during acute pain as compared to rest. This may reflect that externally induced pain inhibits fibromyalgic pain and syndrome-related evaluative processes located in the retrosplenial cortex, and that fibromyalgic pain results from exaggerated attention to sub-noxious pain signaling, that is, secondary hyperalgesia..
In contrast, the parahippocampal cortex and the medial prefrontal network are connected with the dorsal TG, the rostral superior temporal gyrus (STG) and dorsal bank of STS, and the retrosplenial cortex..
The results showed that a large bilateral network supports autobiographical memory: temporal lobe, temporo-parieto-occipital junction, dorsal prefrontal cortex, medial frontal cortex, retrosplenial cortex and surrounding areas, and MTL structures.
The GM was reduced in the posterior cingulate/retrosplenial cortex and superior temporal gyrus of unmedicated BD subjects relative to medicated BD subjects and in the lateral orbital cortex of medicated BD subjects relative to controls.
Changes in morphology were compared in layer V pyramidal cells from medial prefrontal cortex, which sustained the greatest dopamine depletion, and in layer II/III pyramidal cells from retrosplenial cortex, which sustained the greatest choline acetyltransferase depletion.
In accordance with this c-Fos expression difference, the retrosplenial cortex of the trained animals contained significantly more neurons with lever-press-related activity than the motor cortex.
In contrast, spinal cord injury (SCI) resulted in strain-specific changes in forebrain activation categorized by structures that showed significant increases in: (1) only LE SCI rats (posterior, ventrolateral, and ventroposterolateral thalamic nuclei); (2) only SD SCI rats (anterior-dorsal and medial thalamus, basolateral amygdala, cingulate and retrosplenial cortex, habenula, interpeduncular nucleus, hypothalamic paraventricular nucleus, periaqueductal gray); or (3) both strains (arcuate nucleus, ventroposteromedial thalamus, SI and SII somatosensory cortex).
In contrast, the neocortical area 17 and the lateral part of the perirhinal cortex (area 36) were innervated by evenly distributed fine fibers with a moderate number of small varicosities and few ramifications, whereas, the retrosplenial cortex (areas 29e, 29ab and 29cd), and the medial part of the perirhinal cortex (area 35) displayed an intermediate innervation pattern, probably reflecting the transitional nature of these areas being located between the paleo- and the neocortex.
The lowest signal occurred in the retrosplenial cortex.
Human posterior cingulate cortex (PCC) and retrosplenial cortex (RSC) form the posterior cingulate gyrus, however, monkey connection and human imaging studies suggest that PCC area 23 is not uniform and atlases mislocate RSC.
Activation of the retrosplenial cortex but not the amygdala was also observed during the learning process.
Electrical stimulation of the reticular nucleus of the rat thalamus results in activation of c-fos immunoreactivity in nerve cells of the ipsilateral retrosplenial cortex. The c-fos immunoreactive neurons are mainly concentrated in lamina IV of the retrosplenial cortex. Conversely, electrical stimulation of the retrosplenial cortex induced c-fos immunoreactivity in the ipsilateral reticular nucleus of the thalamus.
After pretreatment, animals were injected with MK-801, killed 24 h after the MK-801, and injury to retrosplenial cortex assessed by neuronal Hsp70 protein expression.
Although the parietal lobe is not traditionally thought to support declarative memory, recent event-related fMRI studies of episodic retrieval have consistently revealed a range of memory-related influences on activation in lateral posterior parietal cortex (PPC) and precuneus extending into posterior cingulate and retrosplenial cortex.
By disinhibiting certain multisynaptic circuits, moderate doses of NMDA antagonists produce reversible neurotoxicity in the retrosplenial cortex in rats older than 1 month. Higher doses of these same agents result in the death of neurons in the retrosplenial cortex and several other brain regions. Quantification of the severity of neurodegeneration with stereology revealed that the retrosplenial cortex, induseum griseum, and dentate gyrus had decreasing amounts of damage with decreasing age and onset of sensitivity around PND30.
It has been shown that neurotrophins play important roles in the development and plasticity of thalamic axon innervation into the visual and retrosplenial cortex.
This brain imaging finding was further supported by a microdialysis experiment in rats showing that ketamine increased the extracellular dopamine concentration by up to 200% in the retrosplenial cortex.
Since other limbic structures which are intricately connected with the hippocampal formation, also play an important role in behavioural and neuroendocrine functions, we here used magnetic resonance imaging (MRI) to analyse how two of these areas, the anterior cingulate and retrosplenial cortex, respond to chronic alterations of adrenocortical status: hypocortisolism (induced by adrenalectomy, ADX), normocortisolism (ADX with low-dose corticosterone replacement), and hypercortisolism (ADX with high-dose dexamethasone supplementation). In contrast, hypercortisolism did not influence the volume of the adjacent retrosplenial cortex. The volumes of the anterior cingulate gyrus and retrosplenial cortex were unaffected by the absence of adrenocortical hormones.
Voxel-based analysis of activation patterns in young subjects identified activation in the hippocampus and parahippocampal gyrus, retrosplenial cortex, right and left lateral parietal cortex, medial parietal lobe and cerebellum. In comparison to younger subjects, elderly participants showed reduced activation in the hippocampus and parahippocampal gyrus, medial parietal lobe and retrosplenial cortex.
Areas showing significant deficits included the piriform cortex, neocortex, retrosplenial cortex and certain regions of the hippocampus.
The retrosplenial cortex is located at a critical juncture between the visual cortex and hippocampal formation. Functions of the retrosplenial cortex at the local circuit level, however, remain unclear. Herein, we show how signals traveling from the visual cortex behave in local circuits of the retrosplenial cortex, using optical recording methods and application of caffeine to rat brain slices. These input and output relationships indicate that the retrosplenial cortex may represent an important relay station between the visual cortex and hippocampal formation..
the supracallosal parts of the anterior cingulate and retrosplenial cortices with a general rostro-caudal topography, in the sense that the rostral part of the anterior cingulate cortex and caudal part of the retrosplenial cortex are interconnected and the same holds true for the caudal part of the anterior cingulate cortex and rostral part of the retrosplenial cortex.
A significant main effect of familiarity with greater activation in the familiar (FP and FO) than unfamiliar (UP and UO) trials was observed in the mid-dorsal PCC (mPCC), retrosplenial cortex, posterior precuneus, and the left intraparietal sulcus. Together with data from previous functional imaging studies, the results suggest a functional segregation of human PCC with differential involvement of pPCC in spatial representations of personally familiar places and of the mPCC and retrosplenial cortex in episodic retrieval of personally familiar places and objects.
Thus, in contrast to untrained rats, 5-HT(1A) receptor expression of autoshaping trained rats was augmented in the tubercule olfactory, septal nucleus, nucleus accumbens, caudate putamen, globus pallidus, striate, and parietal (1 and 2), temporal cortex (1 and 3), granular retrosplenial cortex (1), amygdala, and median and dorsal raphe nuclei. There were significant differences between passive vs trained groups, but not regarding untrained rats, in the lateral olfactory tract, dentate gyrus, CA3 area, ventromedial hypothalamic, lateral hypothalamus, preoptic medial, frontal cortex (2), granular retrosplenial cortex (2), entorhinal cortex (1 and 2), piriform cortex, and substantia nigra.
Damage to the retrosplenial cortex (RC) impairs the performance of rodents on spatial learning and memory tasks, but the extent of these deficits was previously reported to be influenced by the lesion type, rat strain, and behavioral task used.
Comparison of recall after instruction in the method of loci with that before it showed significant activation in the left parahippocampal gyrus/retrosplenial cortex/cingulate gyrus/lingual gyrus, left precuneus, left fusiform gyrus, and right lingual gyrus/cingulate gyrus. The present study demonstrated the changes in brain activation pattern associated with the use of the method of loci; left fusiform and lingual activity was associated with both the encoding and recall phases, bilateral prefrontal activity with the encoding phase, and activity of the posterior part of the parahippocampal gyrus, retrosplenial cortex, and precuneus with the recall phase.
The non-competitive NMDA receptor antagonists, including PCP (phencyclidine), ketamine, and MK-801 (dizocilpine) produce psychosis in humans and injure neurons in retrosplenial cortex in adult rodent brain. Systemic injections of mGlu2/3 agonist LY379268, but not mGlu2/3 antagonist LY341495, decreased the injury in the retrosplenial cortex produced by systemic MK-801 as assessed by Hsp70 induction. Bilateral injections of LY379268, but not vehicle, into retrosplenial cortex or bilateral injections of LY379268 into anterior thalamus also decreased the injury in retrosplenial cortex produced by systemic MK-801. The data show that bilateral activation of mGlu2/3 glutamate receptors in cortex or anterior thalamus decreases the neuronal injury in retrosplenial cortex produced by systemic MK-801.
Schizophrenia patients also showed abnormal lateralization of white matter volumes in retrosplenial cortex (area 30) and had lower correlations between frontal and anterior cingulate regions than controls.
A region lateral to the intraparietal sulcus [ inferior parietal lobule complex (IPLC)] and two regions in the medial PPC [ precuneus complex (PCC) and posterior cingulate/retrosplenial cortex (pC/Rsp)] showed strong retrieval success effects for both picture and sound stimuli.
Overall comparisons between encoding and control conditions identified activation in medial frontal gyrus, retrosplenial cortex and posterior inferior parietal cortex.
Activations were observed in the subcallosal cingulate gyrus, prefrontal anterior cingulate, retrosplenial cortex, hippocampus, anterior insula, and nucleus accumbens.
METH was also more toxic than MDMA to dopamine terminals in the habenula, and posterior retrosplenial cortex.
In their review on the retrosplenial cortex Harker and Whishaw [ Neurosci Biobehav Rev, 2004] claim that there is continued disagreement over the importance of this region for navigation. In this reply, evidence is provided showing that Harker and Whishaw [ Neurosci Biobehav Rev, 2004] have created a misleading impression and, in fact, there is a clear consensus that the rat retrosplenial cortex is necessary for navigation.
retrosplenial cortex (RS) is situated both anatomically and functionally between neocortical and limbic structures involved in spatial navigation.
Through separate mechanisms, Alzheimer's disease preferentially affects the medial temporal lobe and cortical networks, including posterior cingulate and retrosplenial cortex early in its progression, often before clinical symptoms are recognized.
In the present study, phosphorylation of cAMP-response element binding protein (pCREB) and expression of c-Fos were measured in the dorsal and ventral hippocampus, as well as in a control region, the retrosplenial cortex, of rats following acquisition and recall of a socially transmitted food preference (STFP). There were no differences in either c-Fos-ir or pCREB-ir in comparisons between trained and control rats in the retrosplenial cortex.
The following regions were engaged to varying degrees depending on the processing demands of each task: retrosplenial cortex, believed to be involved in assigning directional significance to locales within a relatively allocentric framework; medial and posterior parietal cortex, concerned with processing space within egocentric coordinates during imagined movement; and regions of prefrontal cortex, present in tasks heavily dependent on working memory.
Treatment with memantine, 20 mg/kg/day during 14 days, significantly increased the number of [ (125)I]alphabungarotoxin (alpha7 nAChR) binding sites in the frontal- and retrosplenial cortex of hAChE-Tg mice and synaptophysin- and LMW MAP-2 levels in the cortex of both hAChE-Tg and FVB/N controls.
The present study: (1) tested the importance of the retrosplenial cortex for learning a specific heading direction and distance and, (2) determined if lesion size could explain apparent inconsistencies in the results of different research groups. Dark agouti rats received either 'complete' cytotoxic retrosplenial cortex lesions or 'standard' lesions, the latter sparing the caudal retrosplenial cortex. These findings show that lesion size is a critical factor and may explain why some studies have failed to find comparable deficits after retrosplenial cortex lesions..
The retrosplenial cortex, which is situated in a critical position in the flow of information between the hippocampal formation and the neocortex, contributes to spatial memory, but no studies have examined the distinct contribution of each area of the retrosplenial cortex to this behavior. The data highlight the unique and complex contribution of each area of the retrosplenial cortex to behavior..
Injections of Fluorogold into the striatum gave rise to retrograde labeling of PV-positive neurons in the retrosplenial cortex and somatosensory cortex.
We also highlight a network of brain regions, including the left prefrontal cortex, the retrosplenial cortex, the temporo-parietal junction, the caudate and the right cerebellum, which is activated in association with successful recognition of famous faces.
Lesions involving the anterior thalamic nuclei stopped immediate early gene (IEG) activity in specific regions of the rat retrosplenial cortex, even though there were no apparent cytoarchitectonic changes. Granular (caudal granular cortex and rostral granular cortex), but not dysgranular (dysgranular cortex), retrosplenial cortex showed a striking loss of Fos-positive cells. Anterior thalamic lesions (Experiment 3) led to a pronounced IEG decrease of both Fos and zif268 throughout the retrosplenial cortex that now included the dysgranular area. Lesions of the postrhinal cortex (Experiment 4) did not bring about a loss of retrosplenial IEG activity even though this region is also reciprocally connected with the retrosplenial cortex.
RESULTS: RCPM score was significantly positively correlated with the FDOPA Ki in the left hippocampus and with the rrCMRglc in the left middle frontal gyrus and right retrosplenial cortex.
This study was aimed at comparing the effects of damage to the entorhinal cortex and retrosplenial cortex on exploration and reaction-to-change in rats. Both entorhinal cortex lesions and retrosplenial cortex lesions elicited a deficit in the rat's reaction to a spatial change. Overall, these results suggest that the entorhinal cortex and the retrosplenial cortex contribute to the processing of the geometric properties of the environment and have thus close functional links..
By contrast, retrosplenial cortex was more active for recent events regardless of memory vividness.
As a result, more Fos-LI neurons were observed in anterior cingulate cortex, retrosplenial cortex, insular cortex, parietal cortex area 2, frontal cortex area 1-3, claustrum, lateral septal area, amygdala, dorsomedial hypothalamic nucleus, central medial nucleus, paraventricular nucleus, superior colliculus, inferior colliculus and periaqueductal gray.
The retrosplenial cortex (areas 29a-29d) has been implicated in spatial memory, which is essential for performing spatial behavior.
MAP2 mRNA was increased modestly in the dentate gyrus and retrosplenial cortex by chlorpromazine, risperidone, and olanzapine and in the occipitoparietal cortex by chlorpromazine, haloperidol, and risperidone.
Namely, the retrosplenial cortex appears to be involved in evaluating the emotional salience of information from external sources, whereas the rostral frontal cortex also plays a role in internal generation of words with emotional connotation.
The transverse relaxation time T(2), an intrinsic MR parameter thought to reflect impaired cell physiology, was significantly reduced in the hippocampus, cingulate, and retrosplenial cortex, but not the corpus callosum, of PS-APP mice compared to NTg.
Neuroserpin RNA levels are down-regulated in cortical layers II/III and VIa, the hippocampus, the retrosplenial cortex and the medial habenular nucleus, but not in cortical layer V or other areas of the hypothyroid rat brain.
These learning-dependent biochemical events appear to be spatiotemporally controlled, because they do not occur in another brain region involved in learning, the retrosplenial cortex, and at the level of protein expression they show extinction 1 month after training despite memory retention.
Increased cleaved caspase-3 expression was observed at the 24-h time point for both ethanol- and cocaine-exposed brains, most notably in the septum, retrosplenial cortex, and the hippocampus.
The rats were then retested after receiving cytotoxic hippocampal or retrosplenial cortex lesions.
NRHypo neurotoxicity is mediated by a complex disinhibition mechanism in which NMDA antagonists abolish GABAergic inhibition, resulting in the simultaneous excessive release of acetylcholine and glutamate onto the vulnerable retrosplenial cortex (RSC) neurons.
Short-term exposure of adult rats to nitrous oxide (N2O), an inhalational anesthetic and NMDA (N-methyl-D-aspartate) antagonist, causes a reversible neurotoxic vacuole reaction in neurons of the posterior cingulate/retrosplenial cortex (PC/RSC) which resembles that caused by low doses of other NMDA antagonists.
In the granular retrosplenial cortex (GRS) of adult rats, callosally projecting pyramidal neurons in layer 2 form dendritic bundles, 30-100 micro m wide, in layer 1.
The study found that the most consistently hypometabolic region between individual subjects was a subregion of the posterior cingulate, the retrosplenial cortex (BA 29/30). We propose that the retrosplenial cortex may represent a key junction between prefrontal areas involved in implementing retrieval strategies for episodic memory and hippocampal-based mnemonic processing; we therefore interpret the retrosplenial hypometabolism as a probable contributor to the memory impairment seen in mild cognitive impairment by disconnecting these two anatomical networks..
The effects on serotoninergic, noradrenergic and cholinergic markers on neurons of the pontomesencephalic tegmentum nuclei were studied in rats following local administration of fibrillar beta-amyloid peptide (Abeta1-40) into the left retrosplenial cortex. Focal deposition of Abeta in the retrosplenial cortex resulted in a loss of serotoninergic neurons in the dorsal and median raphe nuclei. These results show that three different neurochemically defined populations of neurons in the pontomesencephalic tegmentum are affected by the neurotoxicity of Abeta in vivo and that Abeta might indirectly affect serotoninergic, noradrenergic and cholinergic innervation in the retrosplenial cortex..
In the present study, we examined the effects of LY379268, the group II metabotropic glutamate receptor (mGluR) agonist, on the neuropathological changes in the rat retrosplenial cortex induced by noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine ((+)-MK-801). Administration of LY379268 (1, 3, 10 mg/kg, i.p.) reduced dizocilpine (0.5 mg/kg, i.p.)-induced neuropathological changes in the retrosplenial cortex, in a dose-dependent manner. Furthermore, LY379268 (10 mg/kg, i.p.) significantly reduced the expression of heat shock protein HSP-70, a marker of reversible neuronal injury, in the rat retrosplenial cortex after administration of dizocilpine (0.5 mg/kg, i.p.). Moreover, pretreatment with LY379268 (10 mg/kg, i.p.) significantly suppressed the increase in extracellular acetylcholine (ACh) levels in the retrosplenial cortex induced by administration of dizocilpine (0.5 mg/kg, i.p.). These results suggest that LY379268 has a protective effect on the neurotoxicity in the rat retrosplenial cortex after administration of NMDA receptor antagonists such as dizocilpine..
Noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine ((+)-MK-801) is known to induce neurotoxicity in rat retrosplenial cortex after systemic administration. The present study was undertaken to examine the effects of adenosine A(1) receptor agonists on the neurotoxicity in rat retrosplenial cortex after administration of dizocilpine. Moreover, pretreatment with CCPA (3 mg/kg, i.p.) significantly suppressed the increase of extracellular acetylcholine (ACh) levels in the retrosplenial cortex by administration of dizocilpine (0.5 mg/kg). In contrast, local perfusion of CCPA (1 microM) into the retrosplenial cortex via the dialysis probe did not alter the ACh levels by administration of dizocilpine (0.5 mg/kg), suggesting that the locus of action of CCPA is not in the retrosplenial cortex. These findings suggest that adenosine A(1) receptors agonists could protect against neuropathological changes in rat retrosplenial cortex after administration of the NMDA receptor antagonist dizocilpine..
An area in the right anterior frontal lobe showed an increase in perfusion with age only in the HMPAO group, whereas areas in the bilateral retrosplenial cortex showed decreases in perfusion with age only in the ECD group; neither group showed corresponding changes in the grey matter.
An anxiogenic or a pharmacological stressor, N-methyl-beta-carboline-3-carboxamide (FG-7142), (20 mg/kg, intraperitoneally injected) induced a dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, cingulate and retrosplenial cortex, layers II-VI of the neocortex, lateral habenula, lateral septum, paraventricular nucleus of the thalamus, striatum, central and medial nucleus of the amygdala, but a sparse c-Fos immunostaining in the hippocampus and layer I of the neocortex in the forebrain of 56-day-old rats.
We investigated the cortical afferents of the retrosplenial cortex and the adjacent posterior cingulate cortex (area 23) in the macaque monkey by using the retrograde tracers Fast blue and Diamidino yellow. Injections involving the retrosplenial cortex resulted in labeled neurons within the retrosplenial cortex and in areas 23 and 31 (approximately 78% of the total labeled cells). As in the retrosplenial cortex, injections of area 23 led to many labeled neurons in the frontal cortex, although most of these cells were in areas 9 and 46. These connections are consistent with the retrosplenial cortex acting as an interface between the working memory functions in the prefrontal areas and the long-term memory encoding in the medial temporal lobe.
Females showed more prominently posterior cingulate/retrosplenial cortex activation compared to males.
Activation in anterior cingulate complex and posterior cingulate/retrosplenial cortex showed a task x visual field interaction with lower activation for bilateral than unilateral name matches but higher activation for bilateral than unilateral shape matches, which fits the interhemispheric transfer demands in these tasks..
In contrast to the distribution of GABA(B2)R mRNA, GABA(B1)R gave weak signals throughout the thalamus, piriform cortex, and field CA2 of the hippocampus, but strong signals in the septum, superior colliculus, retrosplenial cortex area, and field CA1 of the hippocampus.
Morphometric analyses of the whole brain revealed that, compared with age-matched controls, both groups had bilateral abnormalities in the hippocampus, putamen, and posterior thalamus, as well as in the right retrosplenial cortex.
The brain asymmetry increases significantly with age in the inferior frontal gyrus, anterior insula, anterior cingulate, parahippocampal gyrus, retrosplenial cortex, coronal radiata, and knee region of the internal capsule.
(+)MK-801 evoke neurodegeneration in retrosplenial cortex in rodents. This indicates that (+)MK-801 neurotoxicity in the retrosplenial cortex is connected with subtle alterations in the learning performance that may be seen in some tests only.
Notably, control subjects, but not O.I., also activated at encoding the precuneus and at recognition the retrosplenial cortex.
Our findings indicate that a region in the parahippocampal cortex and a region in the retrosplenial cortex together comprise a system that mediates both spatial and nonspatial contextual processing.
They are capable of protecting mouse striatal dopamine neurons against MPTP-induced toxicity in the caudate, against MK-801-induced apoptosis in the retrosplenial cortex and against DSP-4-induced depletion of naradrenergic axons.
Secondary damage affected distant sites such as the cingulate/retrosplenial cortex, subiculum, frontal cortex, thalamus, hippocampal dentate gyrus and striatum.
Higher rCBF for patients than controls was found bilaterally in the retrosplenial cortex.
N(2)O administration produced significant (P<0.05) dose-related increases of c-Fos expression in several forebrain regions, including the hypothalamic supraoptic and paraventricular nuclei, the thalamic paraventricular nucleus, the amygdala, and in retrosplenial cortex.
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